2004•Basic medical sciences and clinicsRequires access
Effects of L-arginine on pathologic structure and endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow
Du Jun
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Abstract
To explore the therapeutic effect of L arginine on pathologic structure and endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow. Twenty one SD rats were randomly divided into shunting group (n=7) ,shunting with L arginine group(n=7)and concrol group(n=7).L arginine was orally given in the rats of shunting with L arginine group. An 11 week aortocaval shunting was produced in shunting and shunting with L arginine rats, pulmonary artery mean pressure (mPAP) and the ratio of right ventricular mass to boby weight (RV/BW)and right ventricular mass to left ventricular plus septal mass[RV/(LV+S)] were evaluated. Pulmonary vascular micro and ultra structure were also examined. Meanwhile the concentration of plasma hydrogen sulfide (H 2 S) was measured by spectrophoteries. The activity of CSE in lung tissues was measured by H 2 S production according to chemical analysis. After 11 weeks of aortocaval shunting,we found that pulmonary artery mean pressure was significantly increased. Muscularization of small pulmonary vessels and relative medial thickness of pulmonary arteries were obviously increased in shunting rats as compared with the controls. Ultrastructure of intrapulmonary arteries changed obviously in shunting rats. Meanwhile, plasma H 2 S concentration decreased and the activity of CSE (according to H 2 S production )in lung tissues decreased in shunting rats. However, mPAP and RV/BW,RV/LV+S significantly decreased in rats in shunting with L arginine group as compared with shunt rats( P 0.05).L arginine ameliorated pulmonary vascular structural remodeling in shunting rats in association with a changed endogenous hydrogen sulfide pathway. The result showed that L arginine may play an role in the regulation of development of high pulmonary blood flow induced pulmonary hypertension and pulmonary vascular structural re constructed by changing endogenous H 2 S pathway.